Evaluation of atorvastatin therapy in the OvCa-Chip. (A) Hypothesized signaling and critical molecular events that lead to vascular degradation and platelet extravasation predicted by the OvCa-Chip. It was expected that these pathways and functional consequences would be arrested by atorvastatin treatment through changes in expression of proinflammatory cytokines and genes, such as Src/FAK/ERK, Tie-2, Pyk-1, Rac-1, Akt, and VE-cadherin/β-catenin/VE-PTP. (B) Confocal micrographs showing vascular endothelial junctions (VE-cadherin) in the Control-Chip (top), OvCa-Chip (center), and OvCa-Chip treated with atorvastatin (bottom). Bar represents 200 µm. Quantification of endothelial gaps (C) and expression of major inflammatory cytokines (D) (inset: IL-6 concentration at a reduced scale) released in OvCa-Chip relative to the Control-Chip. (E) Heat map generated from qRT-PCR data showing normalized time-dependent gene expression analysis within Control-Chip, OvCa-Chip, and OvCa-Chip treated with atorvastatin. One-way ANOVA, followed by Dunnett’s multiple-comparisons test. Error bars are the mean ± SEM; n = 3 individual experiments. *P < .05; **P < .01.